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Anoxia‐tolerant Western Painted turtle cortex is also ischemia‐tolerant
Author(s) -
Pamenter Matthew Edward,
Hogg David William,
Gu Xiang Q,
Buck Leslie T,
Haddad Gabriel George
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.711.2
Subject(s) - depolarization , gabaergic , ischemia , turtle (robot) , neuroscience , programmed cell death , inhibitory postsynaptic potential , cortex (anatomy) , biology , membrane potential , chemistry , apoptosis , medicine , endocrinology , biochemistry , fishery
Anoxic or ischemic insults cause immediate hyper‐excitability and cell death in mammalian neurons. Conversely, in Western painted turtle brain, increased GABAergic inhibition suppresses spontaneous electrical activity during anoxia (i.e. spike arrest), and cell death does not occur. To date, the ischemia‐tolerance of turtle neurons has not been investigated, and so to examine this question we treated turtle cortical sheets with a deleterious in vitro mimic of ischemic mammalian brain. We found that ischemia caused: turtle neuronal membrane potential to depolarize from −92 ± 2 to −28 ± 3 mV for the duration of the stress (20 or 60 mins); E GABA to depolarize from −89 ± 1 to −32 ± 3 mV; and input resistance to decrease from 305 ± 33 to 79 ± 12 MΩ. These results suggest that enhanced activation of inhibitory GABAergic mechanisms may also suppress electrical activity in ischemic cortex. Indeed, ischemic neurons were electrically quiet, action potentials could not be elicited, and all changes were reversed to baseline following 20–40 mins re‐perfusion with normoxic ACSF. Furthermore, following 4‐hrs of ischemia, neurons did not exhibit any apparent damage in viability assays; while at 24‐hrs, only early indicators of apoptosis were present. We conclude that anoxia‐tolerant turtle neurons are also ischemia‐tolerant, and that GABAergic inhibition plays a role in this protection.